RESUMO
Pulmonary veno-occlusive disease (PVOD) is a rare but devastating cause of pulmonary hypertension (PH) characterized by preferential remodeling of the pulmonary venules. Mitomycin-C (MMC) is an alkylating agent commonly used in chemotherapy with documented lung toxicity as well as PVOD adverse effect. The incidence of PVOD in patients with anal cancer is much higher than in those with idiopathic PVOD, especially following treatment with MMC. An accurate diagnosis of PVOD can be made based on noninvasive investigations utilizing oxygen parameters, low diffusing capacity for carbon monoxide and characteristic signs on high-resolution computed tomography of the chest. No evidence-based medical therapy exists for PVOD at present and lung transplant remains the preferred definitive therapy for eligible patients. We present a case of autopsy confirmed MMC induced PVOD in a patient with metastatic anal cancer.
RESUMO
BACKGROUND: Concomitant lung/brain traumatic injury results in significant morbidity and mortality. Lung protective ventilation (Acute Respiratory Distress Syndrome Network [ARDSNet]) has become the standard for managing adult respiratory distress syndrome; however, the resulting permissive hypercapnea may compound traumatic brain injury. Airway pressure release ventilation (APRV) offers an alternative strategy for the management of this patient population. APRV was hypothesized to retard the progression of acute lung/brain injury to a degree greater than ARDSNet in a swine model. METHODS: Yorkshire swine were randomized to ARDSNet, APRV, or sham. Ventilatory settings and pulmonary parameters, vitals, blood gases, quantitative histopathology, and cerebral microdialysis were compared between groups using χ2, Fisher's exact, Student's t test, Wilcoxon rank-sum, and mixed-effects repeated-measures modeling. RESULTS: Twenty-two swine (17 male, 5 female), weighing a mean (SD) of 25 (6.0) kg, were randomized to APRV (n = 9), ARDSNet (n = 12), or sham (n = 1). PaO2/FIO2 ratio dropped significantly, while intracranial pressure increased significantly for all three groups immediately following lung and brain injury. Over time, peak inspiratory pressure, mean airway pressure, and PaO2/FIO2 ratio significantly increased, while total respiratory rate significantly decreased within the APRV group compared with the ARDSNet group. Histopathology did not show significant differences between groups in overall brain or lung tissue injury; however, cerebral microdialysis trends suggested increased ischemia within the APRV group compared with ARDSNet over time. CONCLUSION: Previous studies have not evaluated the effects of APRV in this population. While our macroscopic parameters and histopathology did not observe a significant difference between groups, microdialysis data suggest a trend toward increased cerebral ischemia associated with APRV over time. Additional and future studies should focus on extending the time interval for observation to further delineate differences between groups.